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Disruption of cardiac cholinergic neurons enhances susceptibility to ventricular arrhythmias

Nature communications, 2017-01, Vol.8 (1), p.14155-14155, Article 14155

2017

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Protease XIV abolishes NHE inhibition by empagliflozin in cardiac cells

Frontiers in physiology, 2023-07, Vol.14, p.1179131-1179131

2023

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A heterozygous deletion mutation in the cardiac sodium channel gene SCN5A with loss- and gain-of-function characteristics manifests as isolated conduction disease, without signs of Brugada or long QT syndrome

PloS one, 2013-06, Vol.8 (6), p.e67963

2013

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Organ explant culture of neonatal rat ventricles: a new model to study gene and cell therapy

PloS one, 2013-03, Vol.8 (3), p.e59290-e59290

2013

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Two Distinct Congenital Arrhythmias Evoked by a Multidysfunctional Na+ Channel

Circulation research, 2000-05, Vol.86 (9), p.e91-e97

2000

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The opioid tramadol blocks the cardiac sodium channel Nav1.5 in HEK293 cells

Europace (London, England), 2023-08, Vol.25 (9)

2023

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Treatment of Atrial and Ventricular Arrhythmias Through Autonomic Modulation

JACC. Clinical electrophysiology, 2015-12, Vol.1 (6), p.496-508

2015

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Contribution of Sodium Channel Mutations to Bradycardia and Sinus Node Dysfunction in LQT3 Families

Circulation research, 2003-05, Vol.92 (9), p.976-983

2003

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Decreasing microtubule detyrosination modulates Nav1.5 subcellular distribution and restores sodium current in mdx cardiomyocytes

Cardiovascular research, 2024-05, Vol.120 (7), p.723-734

2024

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Is IGF‐1 a useful inhibitor of Na+/H+‐exchanger activity?

Acta Physiologica, 2018-10, Vol.224 (2), p.e13164-n/a

2018

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Functional NaV1.8 Channels in Intracardiac Neurons: The Link Between SCN10A and Cardiac Electrophysiology

Circulation research, 2012-07, Vol.111 (3), p.333-343

2012

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Effects of acetylcholine and noradrenalin on action potentials of isolated rabbit sinoatrial and atrial myocytes

Frontiers in physiology, 2012-01, Vol.3, p.174-174

2012

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Anti-arrhythmic potential of the late sodium current inhibitor GS-458967 in murine Scn5a-1798insD+/- and human SCN5A-1795insD+/- iPSC-derived cardiomyocytes

Cardiovascular research, 2017-06, Vol.113 (7), p.829-838

2017

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Letter by Baartscheer et al Regarding Editorial, “Matter of Fat: Are Lipids Antiarrhythmic?”

Circulation. Arrhythmia and electrophysiology, 2016-03, Vol.9 (3), p.e003933-e003933

2016

Volltextzugriff (PDF)

Ionic mechanism of delayed afterdepolarizations in ventricular cells isolated from human end-stage failing hearts

Circulation (New York, N.Y.), 2001-11, Vol.104 (22), p.2728-2733

2001

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Right ventricular fibrosis and conduction delay in a patient with clinical signs of brugada syndrome : A combined electrophysiological, genetic, histopathologic, and computational study

Circulation (New York, N.Y.), 2005-11, Vol.112 (18), p.2769-2777

2005

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Dyscholesterolemia Protects Against Ischemia-Induced Ventricular Arrhythmias

Circulation. Arrhythmia and electrophysiology, 2015-12, Vol.Publish Ahead of Print (6), p.1481-1490

2015

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Absence of Functional Nav1.8 Channels in Non-diseased Atrial and Ventricular Cardiomyocytes

Cardiovascular drugs and therapy, 2019-12, Vol.33 (6), p.649-660

2019

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Tubulin polymerization modifies cardiac sodium channel expression and gating

Cardiovascular research, 2010-03, Vol.85 (4), p.691-700

2010

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Gender Disparities in Cardiac Cellular Electrophysiology and Arrhythmia Susceptibility in Human Failing Ventricular Myocytes

International Heart Journal, 2005, Vol.46(6), pp.1105-1118

2005

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Overlap syndrome of cardiac sodium channel disease in mice carrying the equivalent mutation of human SCN5A-1795insD

Circulation (New York, N.Y.), 2006-12, Vol.114 (24), p.2584-2594

2006

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Calcium-activated Cl(-) current contributes to delayed afterdepolarizations in single Purkinje and ventricular myocytes

Circulation (New York, N.Y.), 2000-06, Vol.101 (22), p.2639-2644

2000

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Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K + channel

Nature communications, 2018-10, Vol.9 (1), p.4357-15, Article 4357

2018

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A mutation in the human cardiac sodium channel (E161K) contributes to sick sinus syndrome, conduction disease and Brugada syndrome in two families

Journal of molecular and cellular cardiology, 2005-06, Vol.38 (6), p.969-981

2005

Volltextzugriff (PDF)

Conditional immortalization of human atrial myocytes for the generation of in vitro models of atrial fibrillation

Nature biomedical engineering, 2022-04, Vol.6 (4), p.389

2022

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Disruption of cardiac cholinergic neurons enhances susceptibility to ventricular arrhythmias

Protease XIV abolishes NHE inhibition by empagliflozin in cardiac cells

A heterozygous deletion mutation in the cardiac sodium channel gene SCN5A with loss- and gain-of-function characteristics manifests as isolated conduction disease, without signs of Brugada or long QT syndrome

Organ explant culture of neonatal rat ventricles: a new model to study gene and cell therapy

Two Distinct Congenital Arrhythmias Evoked by a Multidysfunctional Na+ Channel

The opioid tramadol blocks the cardiac sodium channel Nav1.5 in HEK293 cells

Treatment of Atrial and Ventricular Arrhythmias Through Autonomic Modulation

Contribution of Sodium Channel Mutations to Bradycardia and Sinus Node Dysfunction in LQT3 Families

Decreasing microtubule detyrosination modulates Nav1.5 subcellular distribution and restores sodium current in mdx cardiomyocytes

Is IGF‐1 a useful inhibitor of Na+/H+‐exchanger activity?

Functional NaV1.8 Channels in Intracardiac Neurons: The Link Between SCN10A and Cardiac Electrophysiology

Effects of acetylcholine and noradrenalin on action potentials of isolated rabbit sinoatrial and atrial myocytes

Anti-arrhythmic potential of the late sodium current inhibitor GS-458967 in murine Scn5a-1798insD+/- and human SCN5A-1795insD+/- iPSC-derived cardiomyocytes

Letter by Baartscheer et al Regarding Editorial, “Matter of Fat: Are Lipids Antiarrhythmic?”

Ionic mechanism of delayed afterdepolarizations in ventricular cells isolated from human end-stage failing hearts

Right ventricular fibrosis and conduction delay in a patient with clinical signs of brugada syndrome : A combined electrophysiological, genetic, histopathologic, and computational study

Dyscholesterolemia Protects Against Ischemia-Induced Ventricular Arrhythmias

Absence of Functional Nav1.8 Channels in Non-diseased Atrial and Ventricular Cardiomyocytes

Tubulin polymerization modifies cardiac sodium channel expression and gating

Gender Disparities in Cardiac Cellular Electrophysiology and Arrhythmia Susceptibility in Human Failing Ventricular Myocytes

Overlap syndrome of cardiac sodium channel disease in mice carrying the equivalent mutation of human SCN5A-1795insD

Calcium-activated Cl(-) current contributes to delayed afterdepolarizations in single Purkinje and ventricular myocytes

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K + channel

A mutation in the human cardiac sodium channel (E161K) contributes to sick sinus syndrome, conduction disease and Brugada syndrome in two families

Conditional immortalization of human atrial myocytes for the generation of in vitro models of atrial fibrillation

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